Dissection versus Prosection: A Comparative Assessment of the Course Experiences, Approaches to Learning, and Academic Performance of Non-medical Undergraduate Students in Human Anatomy.

Many institutions rely upon prosection-based laboratories as more resource-efficient and time-effective alternatives to traditional cadaver dissection for human anatomy education. To facilitate growing enrollment numbers despite resource limitations, the University of Guelph (a non-medical institution) introduced a modified "stepwise" prosection-based laboratory cohort to supplement a dissection-based course. In this design, all students attended the same lectures, but those in the dissection-based cohort learned by performing regional dissections and students in the prosection-based cohort studied from those dissections.

Nitric oxide-mediated promotion of mammary tumour cell migration requires sequential activation of nitric oxide synthase, guanylate cyclase and mitogen-activated protein kinase.

Using clonal derivatives of spontaneous mammary tumours in C3H/HeJ mice, we had earlier shown that tumour-derived nitric oxide (NO), resulting from endothelial type (e) NO synthase (NOS) expression by tumour cells, promoted tumour growth and metastasis by multiple mechanisms: stimulation of tumour cell invasiveness, migration and angiogenesis. Our present study examined the signaling mechanisms underlying NO-mediated promotion of tumour cell migration in a highly metastatic and high eNOS-expressing C3H/HeJ mammary tumour cell line, C3L5. C3L5 cell migration was reduced in the presence of N(G)-nitro-L-arginine methyl ester (L-NAME, NOS inhibitor) in a concentration-dependent manner and restored in the additional presence of excess L-arginine (NOS substrate), confirming a migration-promoting role of endogenous NO.

Role of nitric oxide in tumour progression with special reference to a murine breast cancer model.

Nitric oxide (NO) is a potent bioactive molecule produced in the presence of NO synthase (NOS) enzymes, which mediates numerous physiological functions under constitutive conditions. Sustained overproduction of NO (and NO-reaction products), typically under inductive conditions, can lead to cell cycle arrest and cellular apoptosis. Furthermore, carcinogenesis may result from mutational events following NO-mediated DNA damage and hindrance to DNA repair (e.